Whatcott Clifford, Han Haiyong, Posner Richard G, Von Hoff Daniel D
Clinical Translational Research Division, The Translational Genomics Research Institute (TGEN), Phoenix, Arizona 85004, USA.
Crit Rev Oncog. 2013;18(1-2):135-51. doi: 10.1615/critrevoncog.v18.i1-2.80.
The tumor associated stroma has been described in recent years as being complicit in tumor growth in pancreatic cancer. The stroma hosts a variety of components of both cellular and molecular makeup. In normal tissues, the stroma provides nutrients and regulatory signals for proper cellular polarity and function. However, following oncogenic transformation, the stromal compartment is conscripted to provide stimulatory signals and protection to tumor cells. It is these tumor-stromal interactions that are currently of great therapeutic interest. Several key reports have suggested that therapeutic targeting of the tumor-stromal interactions in pancreatic cancer has the potential to offer survival benefit. In this review, we will discuss the tumor-stromal interactions that contribute to tumor growth and progression, and ways in which we might counter these interactions.
近年来,肿瘤相关基质被认为在胰腺癌的肿瘤生长过程中起到协同作用。基质包含多种细胞和分子组成成分。在正常组织中,基质为细胞的正常极性和功能提供营养和调节信号。然而,在致癌转化后,基质成分被征募来为肿瘤细胞提供刺激信号和保护。正是这些肿瘤-基质相互作用目前引起了极大的治疗关注。几项关键报告表明,针对胰腺癌中肿瘤-基质相互作用进行治疗具有提供生存益处的潜力。在本综述中,我们将讨论促成肿瘤生长和进展的肿瘤-基质相互作用,以及对抗这些相互作用的方法。